Children with obsessive-compulsive disorder: are they just “little adults”?
Simran K. Kalra, Susan E. Swedo
Simran K. Kalra, Susan E. Swedo
Published April 1, 2009
Citation Information: J Clin Invest. 2009;119(4):737-746. https://doi.org/10.1172/JCI37563.
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Children with obsessive-compulsive disorder: are they just “little adults”?

Abstract

Childhood-onset obsessive-compulsive disorder (OCD) affects 1%–2% of children and adolescents. It is characterized by recurrent obsessions and compulsions that create distress and interfere with daily life. The symptoms reported by children are similar to those seen among individuals who develop OCD in adulthood, and the two groups of patients are treated with similar symptom-relieving behavior therapies and medications. However, there are differences in sex ratios, patterns of comorbidity, and the results of neuroimaging studies that might be important. Here we review the diagnosis and treatment of childhood-onset OCD in light of pediatric and adult studies. We also discuss current knowledge of the pathophysiology of the disorder. Despite advances in this area, further research is needed to understand better the etiopathogenesis of the disorder and to develop new, more effective therapeutic options.

Authors

Simran K. Kalra, Susan E. Swedo

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Figure 1

Model for the cortico-striato-thalamo-cortical circuit dysfunction in individuals with OCD.

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Model for the cortico-striato-thalamo-cortical circuit dysfunction in in...
This model outlines the hypothesis that the cortico-striato-thalamo-cortical circuit is dysfunctional in individuals with OCD. Increased glutamatergic signals from the frontal cortex are hypothesized to increase excitation in the striatum, which increases inhibitory GABA signals to the GPi and SNr. (A) One possibility is that this then decreases the inhibitory output via GABA from the GPi and SNr to the thalamus, resulting in thalamic excitatory glutamatergic output to the frontal cortex. This positive feedback loop leads to repetitive thoughts (obsessions) and behaviors (compulsions). An indirect external loop composed of the GPe and subthalamic nucleus (STN) is postulated to contribute to a steady state of excitation/inhibition in this model. (B) A second possibility is that there is an unknown dysfunction at the striatum and GPe. Decreased inhibition on the GPe leads to increased inhibition of the STN, which decreases its excitation of the GPi/SNr. The GPi/SNr then decreases its inhibitory output on the thalamus, resulting in excitatory output to the frontal cortex (adapted from ref. 67).